Coriandrum sativum attenuates microglia mediated neuroinflammation and MPTP-induced behavioral and oxidative changes in Parkinson's disease mouse model.

Coriandrum sativum attenuates microglia mediated neuroinflammation and MPTP-induced behavioral and oxidative changes in Parkinson's disease mouse model.
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DOI:
10.17179/excli2021-3668
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发表时间:
2021
期刊:
影响因子:
4.6
通讯作者:
Kopalli SR
Kopalli SR
中科院分区:
生物学4区
文献类型:
--
作者:
Koppula S;Alluri R;Kopalli SR

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芫荽(科:伞形科; C. sativum)是一种广泛用作香料和传统药物的潜在草药。本文研究了C.研究了大蒜果实提取物(CSE)对脂多糖(LPS)刺激的BV-2小胶质细胞介导的体外神经炎症和1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的帕金森病(PD)动物模型的体内保护作用。CSE(25、50和100 μg/mL)可显著抑制LPS刺激的BV-2小胶质细胞中一氧化氮(NO)、诱导型NO合酶、环氧合酶-2、白细胞介素-6和肿瘤坏死因子-α的升高(p < 0.05 ~ p < 0.001)。此外,CSE抑制BV-2小胶质细胞中LPS诱导的核因子κ-β活化和IκB-α磷酸化。在体内研究中,CSE(100、200和300 mg/kg)改善MPTP(25 mg/kg,i. p.)转棒、被动回避和旷场实验结果显示,大鼠的运动、认知和行为功能均发生显著性变化(P < 0.05 ~ P < 0.001)。MPTP诱导的脑氧化酶水平变化,如超氧化物歧化酶、过氧化氢酶和脂质过氧化反应,在200和300 mg/kg CSE处理后显著恢复(分别为p < 0.01和p < 0.001)。CSE的高效薄层色谱指纹图谱分析显示,槲皮素和山奈酚-3O-葡萄糖苷作为可识别的化合物的几个独特的峰。总之,我们的研究表明,CSE在体外减弱LPS刺激的小胶质细胞中的神经炎症过程,并在体内恢复MPTP诱导的行为缺陷和脑氧化酶状态,证明其在治疗PD中观察到的神经炎症和氧化应激介导的神经变性中的治疗潜力。
Coriandrum sativum Linn. (family: Umbelliferae; C. sativum), is a potential herb widely used as a spice and traditional medicine. In the present work, the effects of C. sativum fruit extract (CSE), against lipopolysaccharide (LPS)-stimulated BV-2 microglia-mediated neuroinflammation in vitro and 1-methyl-4 phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD) animal model in vivo was investigated. LPS-stimulated increase in nitric oxide (NO), inducible NO synthase, cyclooxygenase-2, interleukin-6 and tumor necrosis factor-alpha were significantly (p < 0.05 ~ p < 0.001) inhibited by CSE (25, 50 and 100 μg/mL) in BV-2 microglial cells. Further, CSE inhibited the LPS-induced nuclear factor of kappa-beta activation and IκB-α phosphorylation in BV-2 microglia. In vivo studies, CSE (100, 200 and 300 mg/kg) ameliorated the MPTP (25 mg/kg, i.p.)-induced changes in locomotor, cognitive and behavior functions evaluated by rotarod, passive avoidance and open field test significantly (p < 0.05 ~ p < 0.001). The MPTP-induced changes in brain oxidative enzyme levels such as superoxide dismutase, catalase, and lipid peroxidation were significantly (p < 0.01 and p < 0.001 at 200 and 300 mg/kg, respectively) restored with CSE treatment. High-performance thin-layer chromatography fingerprinting analysis of CSE exhibited several distinctive peaks with quercetin and kaempferol-3O-glucoside as identifiable compounds. In conclusion, our study indicated that CSE attenuated neuroinflammatory processes in LPS-stimulated microglia in vitro and restored the MPTP-induced behavioral deficits and brain oxidative enzyme status in vivo proving its therapeutic potential in the treatment of neuroinflammatory and oxidative stress-mediated neurodegeneration seen in PD.
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期刊: NATURE PROTOCOLS
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